The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform

Bernhard J. Mitterauer - One of the best experts on this subject based on the ideXlab platform.

  • O-38 - Downregulation and Upregulation of glial connexins may cause synaptic imbalances responsible for the pathophysiology of bipolar disorder
    European Psychiatry, 2012
    Co-Authors: Bernhard J. Mitterauer
    Abstract:

    The model of the pathophysiology of bipolar disorder proposed is based on imbalances in tripartite synapses caused by dysregulations of connexin expression in the astrocytic syncytium. If the expression of connexins is downregulated, a compensatory Upregulation of astrocytic receptors may occur responsible for the pathophysiology of depression. Conversely, if the expression of connexins is upregulated, the expression of the astrocytic receptors may be downregulated responsible for the pathophysiology of mania. In depression, a relative lack of neurotransmitters exerts a protracted synaptic information processing, whereas in mania a relative increase of neurotransmitters may accelerate synaptic information processing. In addition, the modulatory role of gliotransmitters may be affected in bipolar disorder. Since the dysregulations of connexins impair the astrocytic syncytium, these disorders could be explanatory for cognitive impairment both in depression and in mania. Finally, the testability of this model is discussed.

  • Downregulation and Upregulation of glial connexins may cause synaptic imbalances responsible for the pathophysiology of bipolar disorder.
    CNS neuroscience & therapeutics, 2010
    Co-Authors: Bernhard J. Mitterauer
    Abstract:

    SUMMARY The model of the pathophysiology of bipolar disorder proposed is based on imbalances in tripartite synapses caused by dysregulations of connexin expression in the astrocytic syncytium. If the expression of connexins is downregulated, a compensatory Upregulation of astrocytic receptors may occur and be responsible for the pathophysiology of depression. Conversely, if the expression of connexins is upregulated, the expression of the astrocytic receptors may be downregulated and be responsible for the pathophysiology of mania. In depression, a relative lack of neurotransmitters exerts a protracted synaptic information processing, whereas in mania a relative increase of neurotransmitters may accelerate synaptic information processing. In addition, the modulatory role of gliotransmitters may be affected in bipolar disorder. Since the dysregulations of connexins impair the astrocytic syncytium, these disorders could be explanatory for cognitive impairment both in depression and in mania. Finally, the testability of this model is discussed.

Hanhong Bae - One of the best experts on this subject based on the ideXlab platform.

  • Developmental- and stress-mediated expression analysis of cinnamoyl-CoA reductase 1 (CCR1) from Hibiscus cannabinus
    Journal of Plant Interactions, 2015
    Co-Authors: Ritesh Ghosh, Bosung Choi, Jonggeun Kim, Mi-jeong Jeong, Tapan Kumar Mohanta, Hanhong Bae
    Abstract:

    Cinnamoyl-CoA reductase (CCR, EC 1.2.1.44) is an important enzyme responsible for lignin biosynthesis in plants that belongs to the family of oxidoreductases. We analyzed developmental, tissue specific, and stress-mediated expression of the HcCCR1 (HM151381) gene from Hibiscus cannabinus. Gene expression analysis revealed that HcCCR1 was highly upregulated in mature leaves of 16-week-old plants. The maximum Downregulation and Upregulation of HcCCR1 was caused by cold and MeJA treatment, respectively. Sequence analysis demonstrated that HcCCR1 protein (ADK24219) contains a conserved NWYCYGK catalytic domain, while bioinformatics prediction indicated the presence of a palmitoylation site in the HcCCR1 protein. Phylogenetic analysis showed that HcCCR1 is more closely related to HcCCR2 (AGJ84130) and AtCCR proteins than CCR-like proteins. Comparative sequence analysis showed presence of significant differences between HcCCR1 and HcCCR2, which are homologs of H. cannabinus. Expression analysis demonstrated tha...

  • RESEARCH ARTICLE Developmental- and stress-mediated expression analysis of cinnamoyl-CoA reductase 1 (CCR1) from Hibiscus cannabinus
    2015
    Co-Authors: Ritesh Ghosh, Bosung Choi, Jonggeun Kim, Mi-jeong Jeong, Tapan Kumar Mohanta, Hanhong Bae
    Abstract:

    Cinnamoyl-CoA reductase (CCR, EC 1.2.1.44) is an important enzyme responsible for lignin biosynthesis in plants that belongs to the family of oxidoreductases. We analyzed developmental, tissue specific, and stressmediated expression of the HcCCR1 (HM151381) gene from Hibiscus cannabinus. Gene expression analysis revealed that HcCCR1 was highly upregulated in mature leaves of 16-week-old plants. The maximum Downregulation and Upregulation of HcCCR1 was caused by cold and MeJA treatment, respectively. Sequence analysis demonstrated that HcCCR1 protein (ADK24219) contains a conserved NWYCYGK catalytic domain, while bioinformatics prediction indicated the presence of a palmitoylation site in the HcCCR1 protein. Phylogenetic analysis showed that HcCCR1 is more closely related to HcCCR2 (AGJ84130) and AtCCR proteins than CCR-like proteins. Comparative sequence analysis showed presence of significant differences between HcCCR1 and HcCCR2, which are homologs of H. cannabinus. Expression analysis demonstrated that the HcCCR1 gene is modulated by different external stresses.

Ritesh Ghosh - One of the best experts on this subject based on the ideXlab platform.

  • Developmental- and stress-mediated expression analysis of cinnamoyl-CoA reductase 1 (CCR1) from Hibiscus cannabinus
    Journal of Plant Interactions, 2015
    Co-Authors: Ritesh Ghosh, Bosung Choi, Jonggeun Kim, Mi-jeong Jeong, Tapan Kumar Mohanta, Hanhong Bae
    Abstract:

    Cinnamoyl-CoA reductase (CCR, EC 1.2.1.44) is an important enzyme responsible for lignin biosynthesis in plants that belongs to the family of oxidoreductases. We analyzed developmental, tissue specific, and stress-mediated expression of the HcCCR1 (HM151381) gene from Hibiscus cannabinus. Gene expression analysis revealed that HcCCR1 was highly upregulated in mature leaves of 16-week-old plants. The maximum Downregulation and Upregulation of HcCCR1 was caused by cold and MeJA treatment, respectively. Sequence analysis demonstrated that HcCCR1 protein (ADK24219) contains a conserved NWYCYGK catalytic domain, while bioinformatics prediction indicated the presence of a palmitoylation site in the HcCCR1 protein. Phylogenetic analysis showed that HcCCR1 is more closely related to HcCCR2 (AGJ84130) and AtCCR proteins than CCR-like proteins. Comparative sequence analysis showed presence of significant differences between HcCCR1 and HcCCR2, which are homologs of H. cannabinus. Expression analysis demonstrated tha...

  • RESEARCH ARTICLE Developmental- and stress-mediated expression analysis of cinnamoyl-CoA reductase 1 (CCR1) from Hibiscus cannabinus
    2015
    Co-Authors: Ritesh Ghosh, Bosung Choi, Jonggeun Kim, Mi-jeong Jeong, Tapan Kumar Mohanta, Hanhong Bae
    Abstract:

    Cinnamoyl-CoA reductase (CCR, EC 1.2.1.44) is an important enzyme responsible for lignin biosynthesis in plants that belongs to the family of oxidoreductases. We analyzed developmental, tissue specific, and stressmediated expression of the HcCCR1 (HM151381) gene from Hibiscus cannabinus. Gene expression analysis revealed that HcCCR1 was highly upregulated in mature leaves of 16-week-old plants. The maximum Downregulation and Upregulation of HcCCR1 was caused by cold and MeJA treatment, respectively. Sequence analysis demonstrated that HcCCR1 protein (ADK24219) contains a conserved NWYCYGK catalytic domain, while bioinformatics prediction indicated the presence of a palmitoylation site in the HcCCR1 protein. Phylogenetic analysis showed that HcCCR1 is more closely related to HcCCR2 (AGJ84130) and AtCCR proteins than CCR-like proteins. Comparative sequence analysis showed presence of significant differences between HcCCR1 and HcCCR2, which are homologs of H. cannabinus. Expression analysis demonstrated that the HcCCR1 gene is modulated by different external stresses.

Antonio Belli - One of the best experts on this subject based on the ideXlab platform.

  • Potentially neuroprotective gene modulation in an in vitro model of mild traumatic brain injury.
    Molecular and Cellular Biochemistry, 2012
    Co-Authors: Valentina Di Pietro, Angela Maria Amorini, Barbara Tavazzi, David A. Hovda, Stefano Signoretti, Christopher C. Giza, Giacomo Lazzarino, Roberto Vagnozzi, Antonio Belli
    Abstract:

    In this study, we investigated the hypothesis that mild traumatic brain injury (mTBI) triggers a controlled gene program as an adaptive response finalized to neuroprotection, similar to that found in hibernators and in ischemic preconditioning. A stretch injury device was used to produce an equi-biaxial strain field in rat organotypic hippocampal slice cultures at a specified Lagrangian strain of 10 % and a constant strain rate of 20 s(-1). After 24 h from injury, propidium iodide staining, HPLC analysis of metabolites and microarray analysis of cDNA were performed to evaluate cell viability, cell energy state and gene expression, respectively. Compared to control cultures, 10 % stretch injured cultures showed no change in viability, but demonstrated a hypometabolic state (decreased ATP, ATP/ADP, and nicotinic coenzymes) and a peculiar pattern of gene modulation. The latter was characterized by Downregulation of genes encoding for proteins of complexes I, III, and IV of the mitochondrial electron transport chain and of ATP synthase; Downregulation of transcriptional and translational genes; Downregulation and Upregulation of genes controlling the synthesis of glutamate and GABA receptors, Upregulation of calmodulin and calmodulin-binding proteins; proper modulation of genes encoding for proapoptotic and antiapoptotic proteins. These results support the hypothesis that, following mTBI, a hibernation-type response is activated in non-hibernating species. Unlike in hibernators and ischemic preconditioning, this adaptive gene programme, aimed at achieving maximal neuroprotection, is not triggered by decrease in oxygen availability. It seems rather activated to avoid increase in oxidative/nitrosative stress and apoptosis during a transient period of mitochondrial malfunctioning.

Markus Steinfath - One of the best experts on this subject based on the ideXlab platform.

  • Isoprenaline-induced increase in the 40/41 kDa pertussis toxin substrates and functional consequences on contractile response in rat heart.
    Naunyn-Schmiedeberg's archives of pharmacology, 1992
    Co-Authors: Ulrike Mende, Thomas Eschenhagen, Birgit Geertz, Wilhelm Schmitz, Hasso Scholz, Jan Schulte Am Esch, Rainer Sempell, Markus Steinfath
    Abstract:

    Chronic β-adrenoceptor stimulation leads to desensitization of the myocardial adenylyl cyclase signalling pathway which includes β-adrenoceptor Downregulation and Upregulation of Gi-protein α-subunits. However, these investigations have mainly been done in cellular preparations. In this study we report that isoprenaline infusion in vivo leads to an increase in myocardial Gia and present evidence for functional consequences of this increase.

  • Isoprenaline-induced increase in the 40/41 kDa pertussis toxin substrates and functional consequences on contractile response in rat heart
    Naunyn-Schmiedeberg's Archives of Pharmacology, 1992
    Co-Authors: Ulrike Mende, Thomas Eschenhagen, Birgit Geertz, Wilhelm Schmitz, Hasso Scholz, Rainer Sempell, Jan Schulte Am Esch, Markus Steinfath
    Abstract:

    Chronic β-adrenoceptor stimulation leads to desensitization of the myocardial adenylyl cyclase signalling pathway which includes β-adrenoceptor Downregulation and Upregulation of G_i-protein α-subunits. However, these investigations have mainly been done in cellular preparations. In this study we report that isoprenaline infusion in vivo leads to an increase in myocardial G_ia and present evidence for functional consequences of this increase. Rats were treated by a 4-day subcutaneous infusion with isoprenaline (2.4 mg/kg·d), propranolol (9.9 mg/kg·d) and triiodothyronine (T_3, 0.5 mg/kg·d) for comparison. Isoprenaline treatment increased the pertussis toxin-sensitive amount of G_ia by 22±6% and decreased β_1- and β_2-adrenoceptor density from 35±4 to 23±6 fmol/mg protein and 24±4 to 8±6 fmol/mg protein, respectively. Contraction experiments on electrically driven papillary muscles revealed that the negative inotropic potency of the M-cholinoceptor agonist carbachol in the presence of isoprenaline was increased as compared to control (mean EC_50-values: 0.04 μmol/l vs. 0.28 μmol/l). All isoprenaline-induced effects were antagonized by simultaneously administered propranolol. T_3 treatment had no influence on the parameters investigated. The results suggest that chronic β-adrenoceptor stimulation desensitizes myocardial adenylyl cyclase by at least two mechanisms: β-adrenoceptor Downregulation leading to diminished signal transduction in the stimulatory pathway and G_iα Upregulation leading to sensitization of the inhibitory pathway. Such adaptation might protect the heart from chronic exposure to catecholamines in heart diseases with elevated plasma catecholamine levels.